scholarly journals Erratum: Demonstration of the absence of intervening sequences within 23S rRNA genes fromCampylobacter lari

2010 ◽  
Vol 50 (2) ◽  
pp. 206-206
Author(s):  
Akihiro Tazumi ◽  
Yuki Kakinuma ◽  
John E. Moore ◽  
Cherie B. Millar ◽  
Ikue Taneike ◽  
...  
2009 ◽  
Vol 49 (4) ◽  
pp. 386-394 ◽  
Author(s):  
Akihiro Tazumi ◽  
Yuki Kakinuma ◽  
John E. Moore ◽  
Cherie B. Millar ◽  
Ikue Taneike ◽  
...  

2008 ◽  
Vol 48 (4) ◽  
pp. 284-292 ◽  
Author(s):  
Akihiro Tazumi ◽  
Tsuyoshi Sekizuka ◽  
John E. Moore ◽  
Cherie B. Millar ◽  
Ikue Taneike ◽  
...  

2008 ◽  
Vol 53 (6) ◽  
pp. 486-492 ◽  
Author(s):  
A. Tazumi ◽  
T. Sekizuka ◽  
J. E. Moore ◽  
B. C. Millar ◽  
I. Taneike ◽  
...  

2006 ◽  
Vol 73 (4) ◽  
pp. 1208-1214 ◽  
Author(s):  
Kamfai Chan ◽  
William G. Miller ◽  
Robert E. Mandrell ◽  
Sophia Kathariou

ABSTRACT Certain Campylobacter strains harbor a transcribed intervening sequence (IVS) in their 23S rRNA genes. Following transcription, the IVS is excised, leading to fragmentation of the 23S rRNA. The origin and possible functions of the IVS are unknown. Furthermore, the distribution of IVS-harboring strains within Campylobacter populations is poorly understood. In this study, 104 strains of Campylobacter coli from turkeys, representing 27 different multilocus sequence typing-based sequence types (STs), were characterized in terms of IVS content and erythromycin susceptibility. Sixty-nine strains harbored IVSs in all three 23S rRNA genes, whereas the other 35 strains lacked IVSs from at least one of the genes. The STs of the latter strains belonged to an unusual cluster of C. coli STs (cluster II), earlier found primarily in turkey strains and characterized by the presence of the C. jejuni aspA103 allele. The majority (66/69) of strains harboring IVSs in all three 23S rRNA genes were resistant to erythromycin, whereas none of the 35 strains with at least one IVS-free 23S rRNA gene were resistant. Cluster II strains could be transformed to erythromycin resistance with genomic DNA from C. coli that harbored IVS and the A2075G transition in the 23S rRNA gene, associated with resistance to erythromycin in Campylobacter. Erythromycin-resistant transformants harbored both the A2075 transition and IVS. The findings suggest that the absence of IVS in C. coli from turkeys is characteristic of a unique clonal group of erythromycin-susceptible strains and that IVS can be acquired by these strains via natural transformation to erythromycin resistance.


1982 ◽  
Vol 10 (5) ◽  
pp. 1607-1624 ◽  
Author(s):  
Kate Loughney ◽  
Elsebet Lund ◽  
James E. Dahlberg

2001 ◽  
Vol 183 (14) ◽  
pp. 4382-4385 ◽  
Author(s):  
Steven T. Gregory ◽  
Jamie H. D. Cate ◽  
Albert E. Dahlberg

ABSTRACT Spontaneous, erythromycin-resistant mutants of Thermus thermophilus IB-21 were isolated and found to carry the mutation A2058G in one of two 23S rRNA operons. The heterozygosity of these mutants indicates that A2058G confers a dominant or codominant phenotype in this organism. This mutation provides a valuable tool for the genetic manipulation of the 23S rRNA genes ofThermus.


2006 ◽  
Vol 50 (1) ◽  
pp. 359-361 ◽  
Author(s):  
Nicole Wolter ◽  
Anthony M. Smith ◽  
David J. Farrell ◽  
Keith P. Klugman

ABSTRACT A macrolide-resistant clinical isolate of Streptococcus pneumoniae with 23S rRNA mutations showed a heterogeneous phenotype and genotype. The mutant 23S rRNA genes from this isolate transformed susceptible strain R6 to resistance. Culture of resistant strain R6 in the absence of antibiotic pressure showed gene conversion to occur between the four 23S rRNA alleles, resulting in reversion to susceptibility with the resistant phenotype showing a fitness cost. These data explain the disappearance on subculture of heterogeneous macrolide resistance in the pneumococcus.


2011 ◽  
Vol 34 (6) ◽  
pp. 462-469 ◽  
Author(s):  
Pelin Yilmaz ◽  
Renzo Kottmann ◽  
Elmar Pruesse ◽  
Christian Quast ◽  
Frank Oliver Glöckner

2000 ◽  
Vol 14 (10) ◽  
pp. 891-894 ◽  
Author(s):  
Diane E Taylor

Resistance ofHelicobacter pylorito antibiotics ranges from 3% to 10% and may exceed these levels in some countries. The pathophysiology of clarithromycin resistance is reviewed, including the mode of action by which the antibiotic inhibits protein synthesis and the mechanism of resistance, which involves a mutation at position 2142 or 2143 in the V loop domain of the 23S rRNA genes. Mutations of A2142G confer a higher minimum inhibitory concentration than mutations of A2143G. The former demonstrate cross-resistance to macrolide, lincosamide and streptogramin antibiotics, whereas the latter are susceptible to streptogramin B. In vitro mutagenesis combined with natural transformation were used to create several types of clarithromycin-resistant mutants.H pyloristrains with A2142G and A2143G mutations had a higher growth rate than those with A2142C, A2143 or A2142T mutations. Data from this study indicate why clarithromycin-resistant clinical isolates ofH pyloriare more likely to have A2142G or A2143G mutations and only occasionally A2142C mutations.


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